ArticleGenes, chromosomes & cancer2010
Overexpression of dicer as a result of reduced let-7 MicroRNA levels contributes to increased cell proliferation of oral cancer cells.
Article in Genes, chromosomes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 114 citations in OpenAlex.
- Keratinization-associated miR-7 and miR-21 regulate tumor suppressor reversion-inducing cysteine-rich protein with kazal motifs (RECK) in oral cancer.The Journal of biological chemistry · 2012Trial
- How Do DICER1 Syndrome Mutations Disrupt Catalysis? Unveiling Dicer Metal Binding Architecture and Mechanism of Action Using MD Simulations and QM/MM Calculations.Journal of computational chemistry · 2026Article
- The role of microRNAs in modulating Wnt signaling pathway dynamics and their therapeutic implications in non-small cell lung cancer.Discover oncology · 2026Review
- Let-7 miRNAs are Selectively Sensitive to Dicer Dosage.microPublication biology · 2026Article
- Dicer and microRNA-155 dysregulation in multiple sclerosis: biomarkers for disease progression and treatment response.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Molecular and Therapeutic Roles of Non-Coding RNAs in Oral Cancer-A Review.Molecules (Basel, Switzerland) · 2024Review
- Epigenetic Regulation in Oral Squamous Cell Carcinoma Microenvironment: A Comprehensive Review.Cancers · 2023Review
- MYCN mRNA degradation and cancer suppression by a selective small-molecule inhibitor in MYCN-amplified neuroblastoma.Frontiers in oncology · 2022Article
- Epstein-Barr Virus BGLF2 commandeers RISC to interfere with cellular miRNA function.PLoS pathogens · 2022Article
- Aberrant Expression of microRNA Clusters in Head and Neck Cancer Development and Progression: Current and Future Translational Impacts.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Deficiency of DICER reduces the invasion ability of trophoblasts and impairs the pro-angiogenic effect of trophoblast-derived microvesicles.Journal of cellular and molecular medicine · 2020Article
- Article
- Overexpressed miR-200a promotes bladder cancer invasion through direct regulating Dicer/miR-16/JNK2/MMP-2 axis.Oncogene · 2020Article
- Article
- MDA-7/IL-24 regulates the miRNA processing enzyme DICER through downregulation of MITF.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Article
- Cell Cycle Regulation of Stem Cells by MicroRNAs.Stem cell reviews and reports · 2018Review
- A Looking-Glass of Non-coding RNAs in oral cancer.International journal of molecular sciences · 2017Review
- Preferential microRNA targeting revealed by in vivo competitive binding and differential Argonaute immunoprecipitation.Nucleic acids research · 2017Article
- Identification of candidate genes for devil facial tumour disease tumourigenesis.Scientific reports · 2017Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Recent reports have demonstrated that Dicer, an RNase III endonuclease required for microRNA (miRNA) maturation, is aberrantly expressed in different types of cancer. Furthermore, Dicer has been reported to be regulated by the let-7 family of miRNA genes. We hypothesize that Dicer is aberrantly expressed in oral cancer cells due to altered expressions of let-7 and that Dicer contributes to the development and progression of the disease. Western blot examination of Dicer protein levels in four head and neck squamous cell carcinoma (HNSCC) cell lines, including two oral cancer cell lines, demonstrated that Dicer had between 4- and 24-fold higher expression levels when compared to normal human primary gingival epithelial cells. Furthermore, five of six oral cancer tissues analyzed by indirect immunofluorescence had increased Dicer protein expression, compared to normal gingival epithelial tissue. The Dicer mRNA levels were not found to correlate well with protein expression in the HNSCC cell lines, suggesting that Dicer protein expression was post-transcriptionally regulated. Analysis of let-7a and let-7b levels in HNSCC cell lines by real-time PCR demonstrated that let-7b, but not let-7a, was significantly reduced in the HNSCC cell lines compared to control cells. Lastly, transfection of oral cancer cells with chemically synthesized let-7b and small interfering RNAs targeting Dicer significantly inhibited cell proliferation up to 83% and >100%, respectively, as early as 3 days post-transfection. Together, these data demonstrate that elevated expression levels of Dicer in oral cancer cells correlate with downregulation of let-7b and increased cell proliferation.
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